Cardiac electrophysiology refers to the orchestration of electrical pulses that cause the myocardium to contract in a coordinated manner to efficiently pump blood into the arterial tree. Suboptimal physiological alterations that effect the cardiac myocyte milieu can compromise the myocyte function and adversely affect the electrical conduction tissue. As a result, the electrical pulse sequences of the heart may be altered leading to abnormal cardiac sinus rhythms that can cause dysynchronous or suboptimal myocardial contractile behaviors.
Contractile abnormalities, as observed in electrocardiography (ECG) traces, can be characterized as irregular heartbeats or arrhythmias that may manifest as tachycardia, bradycardia, palpitations, or fibrillation. Practitioners having domain expertise in electrocardiology may be able to differentiate abnormal ECG patterns from normal ECG patterns. Practitioners may also be adept at recognizing specific types of arrhythmias via PQRST ECG tracing patterns or behaviors. These ECG patterns provide information regarding the nature or cause of the arrhythmia thereby enabling more effective cardiac health treatment management. For example, arrhythmias can be used to identify numerous forms of physiological dysfunction that include thyroid dysfunction, anemia, myocardial ischemic conditions, and multiple electrical pathways that result in poor cardiac function. In these examples, the recognition of an arrhythmia serves as part of a patient assessment to either diagnose a pathology, thereby enabling its treatment, or to predict onset of a pathology, thereby enabling overall patient management.
Alternatively, cardiac arrhythmias can result from myocardial ischemic conditions and result in decreased cardiac output. Decreased cardiac output may contribute to a hemodynamically unstable physiological state and predispose a patient to life threatening conditions. As such, a second purpose of arrhythmia detection may be to serve as part of a real-time hemodynamic monitoring tool. Integral to facilitating this clinical utility is the ability to characterize the dysrhythmia behavior in terms of the severity of its adverse effect on cardiovascular hemodynamics. Use of physiological feedback of dysfunctional cardiac behavior in concert with other hemodynamic parameters can provide valuable information to characterize the overall physiologic behavior or state of a patient. Measures related to severity of cardiac related hemodynamic instability measures can provide valuable real-time feedback as a part of a hemodynamic monitor to manage patient stability and/or determine appropriate intervention for this purpose.
Cardiac dysrhythmia may also manifest as bradycardia that can result from a hypovolemic state of the patient. The pathogenesis of a hypovolemic response may initially begin with a rapid parasympathetic response to activate the cardiac compensatory mechanism to defend the arterial system against fluid translocation as a basis to preserve pressure and flow. The rapid parasympathetic response may continue until longer term baroreceptor instigated neural activation occurs and more sustained cardiac and vasomotor compensatory mechanisms are engaged. In some instances, a paradoxical bradycardic response can occur reflective of a sympathetic inhibition (also referred to as a Bezold-Jarische reflex) and vasodilation, which exacerbates the hypotensive response. Such vasodilation can occur in response to various forms of shock. In addition, the vasodilation may occur in end-stage renal disease patients undergoing fluid removal during hemodialysis treatments during which a bradycardia-like response can be observed accompanying an induced hypotensive acute condition.
The pulse waveform obtained from a pulse oximeter, also referred to as a photoplethysmograph, is a mature technology that can be used as a standalone monitor or readily integrated as part of a hemodynamic monitoring system. The photoplethysmograph is not capable of capturing electrophysiological signals. However, measures derived from the pulse waveform can be used to assess changes in tissue perfusion and autonomic nervous system stress patterns based upon temporal alterations of the pulse waveform features. The degree of specific waveform feature abnormality and the frequency of incidence of such anomalous waveform features can be used to recognize patient specific levels of decreasing compensation. Decreased hydrodynamic compensation may be indicative of the severity of the adverse hemodynamic impact resulting from cardiac dysfunction. The resultant clinical utility may be to provide either a standalone hemodynamic monitoring device or a component of a hemodynamic monitoring device that enables real-time feedback as a hemodynamic instability monitor based upon detecting threshold limits in pre-identified photoplethysmograph pulse waveform features.